Sex differences and cardiovascular risk

Cardiovascular risk factors such as diabetes confer differing degrees of risk in men and women.     

Sex hormones and cardiovascular risk

The metabolic effects of sex steroids pertinent to cardiovascular risk are described. These effects are discussed for estrogen inducible proteins, coagulation and fibrinolysis, blood pressure and hypertension, carbohydrate metabolism, lipids and lipoproteins, and vessel walls and local prostaglandins. Also described is the cardioprotection from estrogens and estrogen/progesterone treatment and cardiovascular risk. Oral contraceptive (OC) and cardiovascular risk are also discussed with the following effects identified: the influence on many of the multiple risk factors involved in the development of cardiovascular diseases (i.e., lipids, carbohydrate metabolism, and hemostasis), an association between OC use and thromboembolic accidents, a state of hypercoagulability counterbalanced by increased fibrinolytic activity, venous thrombosis, a relationship with the dosage of androgenic progestogens. no atherogenic origin, no age limit for prescribed, healthy, nonsmoking women, and an increased peripheral insulin resistance. It is concluded that it is rarely inadvisable to prescribe low dose natural estrogens in postmenopausal hormone replacement therapy. Factors contraindicating such use are undiagnosed genital bleeding, an active thrombolic or cardiovascular process, carcinoma of the breast or endometrium, and acute liver failure. Estrogen replacement therapy may exert some cardioprotective effect. When progestogens are added to prevent endometrial carcinoma development, the benefits might be reduced. Low estrogen and low progesterone OC use among healthy, nonsmoking women even in middle age poses no risk of death from cardiovascular disease. Premenopausal women may even be protected from coronary atherosclerosis with estrogen-containing OCs. However, it is advisable that OCs be used with the least possible impact on lipid and carbohydrate metabolism, as well as on hemostasis. For those with some prior cardiovascular risk, there are theoretical advantages at present for use of the new, less, or nonandrogenic progestins in OCs; however, caution is urged and informed consent must be obtained until epidemiological studies support this position.     

Sex hormones, lipoproteins, and cardiovascular risk.

Reduced cardiovascular mortality is evidenced in persons undergoing hormone replacement therapy (HRT). Studying the effects of gonadal steroids on lipoproteins is therefore encouraged, not only because of this important revelation, but also due to the information to be gleaned on lipoprotein metabolism, the large numbers of women taking oral contraceptives and HRT, and the rising demand for the therapy. Thus far, studies have been performed on men and animals. This paper reviews some work on estrogens and androgens, and discusses oral contraceptives, HRT, and lipoproteins. In sum, estrogen administered via any route reduces low density lipoprotein concentrations. Given that animal studies demonstrate the ability of HRT to both inhibit the development of atherosclerosis and alter vasomotor tone in atherosclerotic coronary arteries, women with confirmed coronary disease may also be likely to benefit from the therapy. Greater information should be sought on the benefits of HRT for secondary prevention, therapy effects should be monitored, and the effects of estrogen/progestogen combinations should be investigated.     

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性激素与心血管疾病密切相关。无论男女,雄激素均随年龄增长而下降,且与动脉粥样硬化和冠心病呈负相关。雄激素替代治疗可以改善血脂、血管内皮功能,舒张冠状动脉,缓解心绞痛症状。雌激素通过多个途径对心血管疾病产生影响,绝经后女性心血管事件的发生率迅速升高。雌、孕激素替代治疗(HRT)对心血管疾病的益处与风险存在争议,目前尚无指征采用HRT对绝经期妇女进行心血管疾病的一级或二级预防;对用于缓解更年期症状和防治绝经后骨质疏松症,则需权衡利弊,结合患者具体情况进行个体化治疗。     

Sex differences in the impact of nonalcoholic fatty liver disease on cardiovascular risk factors

Background and aims

Information on sex differences in the association of nonalcoholic fatty liver disease (NAFLD) with cardiovascular disease (CVD) risk factors is scarce. We examined whether men exhibit greater differences in established CVD risk factors between NAFLD and non-NAFLD than women.

Hyperglycaemia and cardiovascular risk

Cardiovascular diseases represent, today, the principal cause of mortality in the general population, especially in subjects with type 2 diabetes mellitus. In these patients the risk of death from cardiovascular diseases is equal to that of non-diabetic subjects with a previous episode of myocardial infarction. Many factors concur to determine such high risk. Hyperglycaemia contributes to the increase in morbidity and cardiovascular mortality associated with diabetes mellitus. Hyperglycaemia acts as a multiplier of cardiovascular risk due to frequent association of multiple risk factors in diabetic patients. Therefore, effective treatment requires a more complete assessment of quantitative and qualitative aspects of glycemic control as well as all components of the diabetic syndrome or, more commonly, metabolic syndrome.     

Testosterone and cardiovascular risk

Cardiovascular (CV) disease is one of the most common causes of death in the western populations and, nowadays, its incidence is increasing even in the developing countries; although CV disease affects both sexes, it is more frequent in males in whom it shortens the average life expectancy. In this regard, this difference has been wrongly attributed for many years to the negative effects of testosterone (T); however, nowadays, a large amount of evidence suggests that this hormone may have protective effects on the CV system and that, indeed, the low levels of T could be associated with an increased CV risk and with an augmentation of morbidity and mortality in males. Such an aspect gains great relevance in light of the consideration that T decrease, besides occurring as a consequence of rare pathological conditions, can often take place with natural aging, causing a state of “male menopause”, also called late-onset hypogonadism. In this review, we aimed to summarize the present state of the art concerning the association between T deficit and CV disease by analyzing the protective role of T on CV system and the relationship of this hormonal lack with metabolic syndrome, CV morbidity and mortality, and with the CV complications, such as ischemic heart disease, heart failure and stroke, that frequently occur in T deficiency.     

Glucose and cardiovascular risk

The American Diabetes Association and the World Health Organisation have recently redefined the spectrum of abnormal glucose tolerance. The criteria for diabetes mellitus were sharpened and impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) were classified as intermediate stages between normal glucose homeostasis and diabetes, based on fasting and challenged glucose levels, respectively. Criteria were established for 'the metabolic syndrome', as a cluster of cardiovascular risk factors that frequently coincides with the abnormal glucose tolerance state. The extent to which the glucose level itself should be regarded as a cardiovascular risk factor is the subject of ongoing debate. Recent research suggests that cardiovascular risk is related to the plasma glucose level even in the normal range of glucose concentrations. The impact of glucose in relation to cardiovascular events is discussed in this review.     

Chemokines and cardiovascular risk

Based on the importance of inflammation in atherogenesis, recent work has focused on whether plasma markers of inflammation can noninvasively diagnose and prognosticate atherosclerotic disorders. Although several studies support an important pathogenic role of chemokines in atherosclerosis, potentially representing attractive therapeutic targets in atherosclerotic disorders, this does not necessarily mean that chemokines are suitable parameters for risk prediction. In fact, the ability to reflect upstream inflammatory activity, stable levels in individuals, and high stability of the actual protein (eg, long half-life and negligible circadian variation) are additional important criteria for an ideal biomarker in cardiovascular disease. Although plasma/serum levels of certain chemokines (eg, interleukin- 8/CXCL8 and monocyte chemoattractant protein-1/CCL2) have shown to be predictive for future cardiac events in some studies, their role as clinical biomarkers is unclear, and their ability to predict subclinical atherosclerosis has been disappointing. Further prospective studies, including a larger number of patients, are needed to make any firm conclusion. Based on the participation of several chemokines in atherogenesis, it is possible that in the future, combined measurements of multiple chemokines could reveal as a "signature of disease" that can serve as a highly accurate method to assess for the presence of atherosclerotic disease.     

Obesity and cardiovascular risk

Obesity has assumed epidemic proportions and is expected to decrease the life expectancy of current and future generations by its cardiovascular complications and other associated chronic diseases. Recognizing the gravity of this trend, the American Heart Association recently identified obesity as an independent and important modifiable risk factor for cardiovascular disease. Obesity is known to cluster with other cardiovascular and metabolic risk factors constituting the cardiometabolic syndrome. The pathophysiogic link between obesity and cardiovascular disease is complex and involves multiple metabolic and inflammatory risk factors. In an attempt to better elucidate this major public health problem, this article reviews obesity as an epidemic, the structural and functional changes in the cardiovascular system as a result of obesity, and the pathophysiology of obesity-related cardiomyopathy. The sheer magnitude of the problem of obesity with its immense cardiovascular consequences warrants immediate intervention.     

Aldosterone and cardiovascular risk

Through its classic effects on sodium and potassium homeostasis, aldosterone, when produced in excess, is associated with the development of hypertension and hence with higher cardiovascular and renal risk. In recent years, experimental and epidemiologic data have suggested that aldosterone also may be linked to high cardiovascular risk independently of its effects on blood pressure. Thus, aldosterone has been associated with obesity and metabolic syndrome in selected populations, and these associations may further contribute to the higher cardiovascular risk of subjects with elevated aldosterone levels. Moreover, aldosterone has been reported to promote inflammation, oxidative stress, and fibrosis in a number of tissues. Clinical evidence indicates that patients with primary hyperaldosteronism have a higher risk of developing cardiovascular and renal complications than patients with essential hypertension who have the same level of blood pressure. Aldosterone receptor blockade has been shown to lower cardiovascular mortality after myocardial infarction and in patients with congestive heart failure. Some studies have also demonstrated that aldosterone blockade could have a favorable impact on the progression of renal disease. However, prospective interventional trials are needed to further evaluate the impact of blockade of aldosterone on cardiovascular risk.